Characterization of the Progressive Skin Disease and Inflammatory Cell Infiltrate in Mice with Inhibited NF-κB Signaling

• Published in: Journal of investigative dermatology Vol. 123; no. 1; pp. 101 - 108
• Main Authors: van Hogerlinden, Max, Rozell, Barbro Lundh, Toftgård, Rune, Sundberg, John P.
• Format: Journal Article
• Language: English
• Published: Danvers, MA Elsevier Inc 01.07.2004; Nature Publishing; Elsevier Limited
• Subjects: Biological and medical sciences; Dermatology; inflammation; IκB; Medical sciences; mice; NF-κB; skin neoplasms; transgenic; IκB; NF-κB; transgenic; skin neoplasms; inflammation; mice; Skin disease; Dermatology; Rodentia; Inflammatory disease; Characterization; Signal transduction; Vertebrata; Infiltrate; Mammalia; Mouse; IκB/inflammation/mice/NF-κB/skin neoplasms/transgenic; Animal; Transcription factor NFκB
• ISSN: 0022-202X; 1523-1747
• DOI: 10.1111/j.0022-202X.2004.22706.x

A growth inhibitory role in skin development for the NF-κB proteins has been established in recent years. We have previously shown that inhibition of NF-κB by overexpression of degradation-resistant IκB-α in the skin results in the development of squamous cell carcinomas (SCC). In this paper, we characterize the progressive skin disease leading to cancer development in mice with inhibited NF-κB signaling in the skin. Increased proliferation and a strong inflammatory response were evident in transgenic skin. A mixed inflammatory cell infiltrate dominated by polymorphonuclear leukocytes was observed in concurrence with an upregulation of the proinflammatory cytokine tumor necrosis factor-α. This genetically engineered mouse mutation may be a useful tool to test the efficacy of cytokine therapies for SCC in the future.